scholarly journals Synergic effect of vitamin A and high-fat diet in adipose tissue development and nuclear receptor expression in young rats

2008 ◽  
Vol 100 (4) ◽  
pp. 722-730 ◽  
Author(s):  
Anabelle Redonnet ◽  
Carine Ferrand ◽  
Céline Bairras ◽  
Paul Higueret ◽  
Catherine Noël-Suberville ◽  
...  

In order to study the effects of dietary lipids and vitamin A on the development of adipose tissues, young rats were submitted for 8 d to a control or to two cafeteria diets with normal (Caf) or higher (Caf+) vitamin A levels. Retinoid (retinoic acid receptor (RAR) α, RARγ, retinoid X receptor (RXR) α) and fatty acid (PPARγ) receptor mRNA was measured in the subcutaneous white adipose tissue (Swat) and in isolated mature adipocytes by RT-PCR. The stroma vascular fraction was cultured in vitro to test the capacities of the adipocyte precursors to proliferate and differentiate. The Caf diet enriched in vitamin A resulted in an increased adiposity, due to increased adipocyte hypertrophy. This was concomitant with a lower expression of RARα and RARγ mRNA ( − 34·6 and − 38·6 %) and a higher expression of PPARγ (+59 %) in the Swat and, to a less extent, in isolated adipocytes. Positive correlations were obtained between PPARγ mRNA and Swat weights and between PPARγ and RXRα mRNA. By contrast, RARγ mRNA and Swat masses were negatively correlated. The adipocyte precursors from Caf+ Swat proliferated more, in vitro, at the beginning of the culture. This difference progressively disappeared and was totally absent after 8 d of culture, but with a higher percentage of differentiated preadipocytes (+80·3 %) in the Caf+ group. In conclusion, lipids and vitamin A act synergistically on the normal growth of the adipose tissue in young rats, concomitant with an imbalance in the pattern of the nuclear receptors. These changes influence the early normal development of the endogenous adipocyte precursors.

Author(s):  
Tammy Ying ◽  
Thea N. Golden ◽  
Lan Cheng ◽  
Jeff Ishibashi ◽  
Patrick Seale ◽  
...  

The cytokine interleukin 4 (IL-4) can increase beige adipogenesis in adult rodents. However, neonatal animals use a distinct adipocyte precursor compartment for adipogenesis compared to adults. In this study, we address whether IL-4 can induce persistent effects on adipose tissue when administered subcutaneously in the interscapular region during the neonatal period in Sprague Dawley rats. We injected IL-4 into neonatal male rats during postnatal days 1-6, followed by analysis of adipose tissue and adipocyte precursors at 2 weeks and 10 weeks of age. Adipocyte precursors were cultured and subjected to differentiation in vitro. We found that a short and transient IL-4 exposure in neonates upregulated uncoupling protein 1 (Ucp1) mRNA expression and decreased fat cell size in subcutaneous white adipose tissue (WAT). Adipocyte precursors from mature rats that had been treated with IL-4 as neonates displayed a decrease in adiponectin (Adipoq) but no change in Ucp1 expression, as compared to controls. Thus, neonatal IL-4 induces acute beige adipogenesis and decreases adipogenic differentiation capacity long term. Overall, these findings indicate that the neonatal period is critical for adipocyte development and may influence the later onset of obesity.


1989 ◽  
Vol 11 (3) ◽  
pp. 1-6 ◽  
Author(s):  
Luigi M. De Luca ◽  
Elizabeth M. McDowell

In this paper we have suggested the new concept of exotrophic cells, i.e. cells that have conditionally escaped the need for an essential nutrient, such as vitamin A. These exotrophs might become fixed by a mutation and eventually contribute to the tumorigenic phenotype. The discovery of the retinoic acid receptor (RAR) has opened up new horizons in the search for the mechanism of action of retinoic acid [17; 18]. It is intriguing that a second retinoic acid receptor, RARE, is abundantly expressed in hepatoma tissue and not in normal liver; Benbrook et al. [191 suggest that the erroneous expression of the RARE might contribute to tumour development in liver. How and whether these findings relate to the vitamin-A-deficient status of hepatoma cells remains to be understood.


2002 ◽  
pp. 87-102 ◽  
Author(s):  
X-k Zhang

Apoptosis represents an effective way to eliminate cancer cells. Unfortunately, advanced prostate tumors eventually progress to androgen-independent tumors, which are resistant to current therapeutic approaches that act by triggering apoptosis. Vitamin A and its natural and synthetic analogs (retinoids) induce apoptosis in prostate cancer cells in vitro and in animal models, mainly through induction of retinoic acid receptor-beta (RARbeta). Expression levels of RARbeta, however, are significantly reduced in hormone-independent prostate cancer cells. Recently, a new class of synthetic retinoids related to 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid (AHPN) (also called CD437) that effectively induces apoptosis of both hormone-dependent and -independent prostate cancer cells in a retinoid receptor-independent manner was identified and has drawn a lot of attention in the field. The apoptotic effect of AHPN requires expression of orphan receptor TR3 (also called nur77 or NGFI-B). Paradoxically, TR3 expression is also induced by androgen and other mitogenic agents in prostate cancer cells to confer their proliferation. The recent finding that TR3 migrates from the nucleus to mitochondria to trigger apoptosis in response to AHPN suggests that the opposing biological activities of TR3 are regulated by its subcellular localization. Thus, agents that induce translocalization of TR3 from the nucleus to mitochondria will have improved efficacy against prostate cancer. TR3, therefore, represents an unexplored molecule that may be an ideal target for developing new agents for prostate cancer therapy.


Molecules ◽  
2021 ◽  
Vol 26 (6) ◽  
pp. 1757
Author(s):  
Michelle Min Fang Yee ◽  
Kok-Yong Chin ◽  
Soelaiman Ima-Nirwana ◽  
Sok Kuan Wong

Vitamin A is a fat-soluble micronutrient essential for growth, immunity, and good vision. The preformed retinol is commonly found in food of animal origin whereas provitamin A is derived from food of plant origin. This review summarises the current evidence from animal, human and cell-culture studies on the effects of vitamin A towards bone health. Animal studies showed that the negative effects of retinol on the skeleton were observed at higher concentrations, especially on the cortical bone. In humans, the direct relationship between vitamin A and poor bone health was more pronounced in individuals with obesity or vitamin D deficiency. Mechanistically, vitamin A differentially influenced the stages of osteogenesis by enhancing early osteoblastic differentiation and inhibiting bone mineralisation via retinoic acid receptor (RAR) signalling and modulation of osteocyte/osteoblast-related bone peptides. However, adequate vitamin A intake through food or supplements was shown to maintain healthy bones. Meanwhile, provitamin A (carotene and β-cryptoxanthin) may also protect bone. In vitro evidence showed that carotene and β-cryptoxanthin may serve as precursors for retinoids, specifically all-trans-retinoic acid, which serve as ligand for RARs to promote osteogenesis and suppressed nuclear factor-kappa B activation to inhibit the differentiation and maturation of osteoclasts. In conclusion, we suggest that both vitamin A and provitamin A may be potential bone-protecting agents, and more studies are warranted to support this hypothesis.


1965 ◽  
Vol 50 (4) ◽  
pp. 648-656 ◽  
Author(s):  
Paul M. Beigelman ◽  
Philip B. Hollander ◽  
David Shube

ABSTRACT In vitro penetrations of rat epididymal adipose tissue by glass microelectrodes, containing 3 m KCl, elicit resting membrane electrical potentials (REP). Adipose tissue REP in young rats is reversibly increased by 1–1000 μU insulin/ml. Insulin antibody, diluted 1/1000–1/4800, significantly inhibits this elevation of REP by insulin.


1969 ◽  
Vol 47 (12) ◽  
pp. 975-980 ◽  
Author(s):  
P. Hahn ◽  
Z. Drahota ◽  
J. Skala ◽  
S. Kazda ◽  
Molly E. Towell

Rats aged 7 to 9 days were injected for 1 to 3 days with 5 mg/100 g body weight cortisone acetate per day. This led to an increase in the weight of brown adipose tissue, an increase in its fat content, and a decrease in its protein content. The content of norepinephrine in brown adipose tissue was decreased by cortisone treatment. The in vitro increase in O2 consumption following the addition of 5 μg nore-pinephrine/ml in vitro to brown adipose tissue from control animals was abolished by cortisone administration. Lipolysis due to norepinephrine was, however, not affected and was even slightly increased in cortisone-treated rats. Mitochondrial succinate–tetrazolium reductase activity was decreased after treatment with cortisone. It is concluded that cortisone alters the mitochondria of brown adipose tissue but has little effect on lipolysis as such. The content of norepinephrine in brown adipose tissue was found to decrease immediately after birth and then to return rapidly to higher levels.


1941 ◽  
Vol 12 (2) ◽  
pp. 109-118 ◽  
Author(s):  
S. N. Ray ◽  
Karam Chand ◽  
K. Govind Rau

1. A simple method is described for the determination of carotene and vitamin A in milk. Figures for the carotene content of milk were higher and those for vitamin A were lower than similar figures reported by Western workers.2. Figures for vitamin C in milk are similar to corresponding figures of English and American workers. Previous low values for vitamin C, reported by Indian workers, are due to destruction of the vitamin by light.3. The vitamin C concentration of milk is not subject to great individual variation, probably because cows cannot excrete in milk any vitamin C taken in with the food and because vitamin C of milk is produced by synthesis within the mammary glands from some simple blood constituents.4. To test the ability of bovines to synthesize vitamin C, young calves were kept for long periods on a strictly vitamin C-free diet. The concentration of vitamin in the blood and other tissues of these animals remained, however, at a normal level. Calves appear therefore to be able to synthesize sufficient vitamin C for their normal growth and activity.5. Unsuccessful attempts were made to produce vitamin C in vitro by growing bacteria isolated from various parts of the alimentary canal on media prepared from ingesta taken from the regions from which they were isolated.


2006 ◽  
Vol 291 (6) ◽  
pp. E1264-E1273 ◽  
Author(s):  
James P. Warne ◽  
Christopher D. John ◽  
Helen C. Christian ◽  
John F. Morris ◽  
Roderick J. Flower ◽  
...  

In this study, epididymal adipose tissue from male annexin 1 (ANXA1)-null and wild-type control mice were used to explore the potential role of ANXA1 in adipocyte biology. ANXA1 was detected by Western blot analysis in wild-type tissue and localized predominantly to the stromal-vascular compartment. Epididymal fat pad mass was reduced by ANXA1 gene deletion, but adipocyte size was unchanged, suggesting that ANXA1 is required for the maintenance of adipocyte and/or preadipocyte cell number. Epididymal tissue from wild-type mice responded in vitro to noradrenaline and isoprenaline with increased glycerol release, reduced IL-6 release, and increased cAMP accumulation. Qualitatively similar but significantly attenuated responses to the catecholamines were observed in tissue from ANXA1-null mice, an effect that was not associated with changes in β-adrenoceptor mRNA expression. Lipopolysaccharide (LPS) also stimulated lipolysis in vitro, but its effects were muted by ANXA1 gene deletion. By contrast, LPS failed to influence IL-6 release from wild-type tissue but stimulated the release of the cytokine from tissue from ANXA1-null mice. ANXA1 gene deletion did not affect glucocorticoid receptor expression or the ability of dexamethasone to suppress catecholamine-induced lipolysis. It did, however, augment IL-6 expression and modify the inhibitory effects of glucocorticoids on IL-6 release. Collectively, these studies suggest that ANXA1 supports aspects of adipose tissue mass and alters the sensitivity of epididymal adipose tissue to catecholamines, glucocorticoids, and LPS, thereby modulating lipolysis and IL-6 release.


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